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Shock. Scott G. Sagraves, MD, FACS Assistant Professor Trauma & Surgical Critical Care Associate Director of Trauma UHS of Eastern Carolina. Objectives. Define & classify shock Outline management principles Discuss goals of fluid resuscitation

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Shock

Shock

Scott G. Sagraves, MD, FACS

Assistant Professor

Trauma & Surgical Critical Care

Associate Director of Trauma

UHS of Eastern Carolina


Objectives

Objectives

  • Define & classify shock

  • Outline management principles

  • Discuss goals of fluid resuscitation

  • Understand the concepts of oxygen supply and demand in managing shock.

  • Describe the physiologic effects of vasopressors and inotropic agents


Goals

Goals

  • Review hemodynamic techniques in the ICU

  • Introduce the concept of the cardiac cycle

  • Review of the pulmonary artery catheter parameters

  • Utilize the presentation to analyze clinical cases and to feel comfortable with pa-c parameters.


Shock1

Shock:

“A momentary pause in the act of death.”

-John Collins Warren, 1800s


Hypotension

Hypotension

  • In Adults:

    • systolic BP  90 mm Hg

    • mean arterial pressure  60 mm Hg

    •  systolic BP > 40 mm Hg from the patient’s baseline pressure


Definition

Definition

SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand.


Hypoperfusion can be present in the absence of significant hypotension

“Hypoperfusion can be present in the absence of significant hypotension.”

-fccs course


Pathophysiology

Pathophysiology

ATP + H2O  ADP + Pi + H+ + Energy

Acidosis results from the accumulation of acid when during anaerobic metabolism the creation of ATP from ADP is slowed.

H+ shift extracellularly and a metabolic acidosis develops


Pathophysiology1

Pathophysiology

  • ATP production fails, the Na+/K+ pump fails resulting in the inability to correct the cell electronic potential.

  • Cell swelling occurs leading to rupture and death.

  • Oxidative Phosphorylation stops & anaerobic metabolism begins leading to lactic acid production.


Why monitor

Why Monitor?

  • Essential to understanding their disease

  • Describe the patient’s physiologic status

  • Facilitates diagnosis and treatment of shock


History

History

  • 1960’s

    • low BP = shock; MSOF resulted after BP restored

  • 1970’s

    • Swan & Ganz - flow-directed catheter

    • thermistor  cardiac output

  • 1980’s

    • resuscitation based on oxygen delivery, consumption & oxygen transport balance.


Pulmonary artery catheter

Pulmonary Artery Catheter


Pulmonary artery catheter1

Pulmonary Artery Catheter

  • INDICATIONS

    • volume status

    • cardiac status

  • COMPLICATIONS

    • technical

    • anatomic

    • physiologic


Placement

PLACEMENT


West s lung zones

West’s Lung Zones

  • Zone I - PA > Pa > Pv

  • Zone II - Pa > PA > Pv

  • Zone III - Pa > Pv > PA

  • PA = alveolar

  • Pa = pulmonary artery

  • Pv = pulmonary vein


Correct pa c position

Correct PA-C Position


Standard parameters

Measured

Blood pressure

Pulmonary A. pressure

Heart rate

Cardiac Output

Stroke volume

Wedge pressure

CVP

Calculated

Mean BP

Mean PAP

Cardiac Index

Stroke volume index

SVRI

LVSWI

BSA

Standard Parameters


Why index

Why Index?

  • Body habitus and size is individual

  • Inter-patient variability does not allow “normal” ranges

  • “Indexing” to patient with BSA allows for reproducible standard


Index example

PATIENT A

60 yo male

50 kg

CO = 4.0 L/min

BSA = 1.86

CI = 2.4 L/min/m2

PATIENT B

60 yo male

150 kg

CO = 4.0 L/min

BSA = 2.64

CI = 1.5 L/min/m2

Index Example


Pa insertion

PA Insertion

20

15

10

5

PA 19/10

PAOP = 9

RA = 5

RV = 22/4

0


Shock

CVP

  • CVP of SVC at level of right atrium

  • pre-load “assessment”

  • normal 4 - 10 mm Hg

  • limited value


Shock

PAOP

  • End expiration

  • Reflection changes with positive pressure

  • Waveforms change  every 20 cm


Waveform analysis

Waveform Analysis

  • A wave - atrial systole

  • C wave - tricuspid valve closure @ ventricular systole

  • V wave - venous filling of right atrium


Cardiac cycle

Cardiac Cycle

PVRI

MPAP

pulmonary

PCWP

Right ventricle

Left ventricle

RVSWI

LVSWI

MAP

CVP

systemic

SVRI


Hemodynamic calculations

Hemodynamic Calculations

ParameterNormal

Cardiac Index (CI)2.8 - 4.2

Stroke Volume Index (SVI)30 - 65

Sys Vasc Resistance Index (SVRI)1600 - 2400

Left Vent Stroke Work Index (LVSWI)43 - 62


Cardiac index

Cardiac Index

C.I. = HR x SVI

SVI measures the amount of blood ejected by the ventricle with each cardiac contraction.

Total blood flow = beats per minute x blood volume ejected per beat


Vascular resistance index

SYSTEMIC (SVRI)

MAP - CVP

CI

 SVR = vasoconstriction

 SVR = vasodilation

PULMONARY (PVRI)

MPAP - PAOP

CI

PVR = constriction

PE, hypoxia

Vascular Resistance Index

x 80

x 80

Vascular resistance = change in pressure/blood flow


Stroke work

Stroke Work

LVSWI = (MAP-PAOP) x SVI x 0.0136

normal = 43 - 62

VSWI describe how well the ventricles are contracting and can be used to identify patients who have poor cardiac function.

ventricular stroke work =  pressure x vol. ejected


Too many numbers

Too Many Numbers


Definitions

Definitions

  • O2 Delivery - volume of gaseous O2 delivered to the LV/min.

  • O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min.

  • O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic manner

Demand > consumption = anaerobic metabolism


Rationale for improving o 2 delivery

Rationale for Improving O2 Delivery

Insult

Tissue Hypoxia

Demands are met

Increased Delivery

Increased Consumption


Critical o 2 delivery

Critical O2 Delivery

VO2I

The critical value is variable

& is dependent upon the patient, disease, and the metabolic demands of the patient.

DO2I


Oxygen calculations

Arterial Oxygen Content (CaO2)

Venous Oxygen Content (CvO2)

Arteriovenous Oxygen Difference (avDO2)

Delivery (O2AVI)

Consumption (VO2I)

Efficiency of the oxygenation of blood and the rates of oxygen delivery and consumption

Oxygen Calculations


Arterial oxygen content

Arterial Oxygen Content

CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031)

If low, check hemoglobin or pulmonary gas exchange


Arteriovenous oxygen difference

Arteriovenous Oxygen Difference

avDO2 = CaO2 - CvO2

Values > 5.6 suggests more complete tissue oxygen extraction, typically seen in shock


Oxygen delivery do 2 i

Oxygen Delivery (DO2I)

O2AVI = CI x CaO2 x 10

Normal values suggests that the heart & lungs are working efficiently to provide oxygen to the tissues.

< 400 is bad sign


Oxygen consumption

Oxygen Consumption

VO2I = CI x (CaO2 - CvO2)

If VO2I < 100 suggest tissues are not getting enough oxygen


Svo 2

SvO2

VO2

SvO2 =

1-

DO2


Oxycalculations

Oxycalculations


Resuscitation goals

Resuscitation Goals

  • CI = 4.5 L/min/m2

  • DO2I = 600 mL/min/m2

  • VO2I = 170 mL/min/m2

NOT ALL PATIENTS CAN ACHIEVE THESE GOALS

Critically ill patients who can respond to their disease states by

spontaneously or artificially meeting these goals do show a

better survival.


Break time

Break Time…


Shock is a symptom of its cause

“Shock is a symptom of its cause.”

-fccs course


Signs of organ hypoperfusion

Signs of Organ Hypoperfusion

  • Mental Status Changes

  • Oliguria

  • Lactic Acidosis


Components

Components


Categories of shock

Categories of Shock

  • HYPOVOLEMIC

  • CARDIOGENIC

  • DISTRIBUTIVE

  • OBSTRUCTIVE


Goals of shock resuscitation

Goals of Shock Resuscitation

  • Restore blood pressure

  • Normalize systemic perfusion

  • Preserve organ function


In general treat the cause

In general, treat the cause...


Hypovolemic shock

Causes

hemorrhage

vomiting

diarrhea

dehydration

third-space loss

burns

Signs

 cardiac output

 PAOP

 SVR

Hypovolemic Shock


Classes of hypovolemic shock

Classes of Hypovolemic Shock


Treatment hypovolemic

Treatment - Hypovolemic

  • Reverse hypovolemia vs. hemorrhage control

  • Crystalloid vs. Colloid

  • PASG role?

  • Pressors?


Resuscitation

Resuscitation

  • Transport times < 15 minutes showed pre-hospital fluids were ineffective, however, if transport time > 100 minutes fluid was beneficial.

  • Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.


Fluid administration

Fluid Administration

  • 1 L crystalloid  250 ml colloid

  • crystalloids are cheaper

  • blood must supplement either

  • FFP for coagulopathy, NOT volume

  • Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused

  • NO survival benefit with colloids


Role of pasg

Roleof PASG?

  • Houston - Higher mortality rate in penetrating thoracic, cardiac trauma

  • No benefit in penetrating cardiac trauma

  • Role undefined in rural, blunt trauma

  • Splinting role


Cardiogenic shock

Cardiogenic Shock

  • Cause

    • defect in cardiac function

  • Signs

    •  cardiac output

    •  PAOP

    •  SVR

    •  left ventricular stroke work (LVSW)


Coronary perfusion pressure

Coronary Perfusion Pressure

Coronary PP = DBP - PAOP

coronary perfusion =  P across coronary a.

GOAL - Coronary PP > 50 mm Hg


The failing heart

The Failing Heart

  • Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient.

  • Fluids first, then cautious pressors

  • Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure)

  • If inotropes and vasopressors fail, intra-aortic balloon pump


Distributive shock

Distributive Shock

  • Types

    • Sepsis

    • Anaphylactic

    • Acute adrenal insufficiency

    • Neurogenic

  • Signs

    • ± cardiac output

    •  PAOP

    • SVR


Sirs distributive shock

SIRS - Distributive Shock

  • Prompt volume replacement - fill the tank

  • Early antibiotic administration - treat the cause

  • Inotropes - first try Dopamine

  • If MAP < 60

    • Dopamine = 2 - 3 g/kg/min

    • Norepinephrine = titrate (1-100 g/min)

  • R/O missed injury


Adrenal crisis distributive shock

Adrenal Crisis Distributive Shock

  • Causes

    • Autoimmune adrenalitis

    • Adrenal apoplexy = B hemorrhage or infarct

    • heparin may predispose

  • Steroids may be lifesaving in the patient who is unresponsive to fluids, inotropic, and vasopressor support. Which one?


Obstructive shock

Obstructive Shock

  • Causes

    • Cardiac Tamponade

    • Tension Pneumothorax

    • Massive Pulmonary Embolus

  • Signs

    •  cardiac output

    •  PAOP

    •  SVR


Endpoints

Endpoints?

  • ACS CoT ATLS - restoration of vital signs and evidence of end-organ perfusion

  • Swan-guided resuscitation

    • C.I.  4.5, DO2I  670, VO2I  166

  • Lactic Acid clearance

  • Gastric pH


Summary

Summary

TypePAOPC.O.SVR

HYPOVOLEMIC 

CARDIOGENIC 

DISTRIBUTIVE  or N varies 

OBSTRUCTIVE   


Vasopressor agents

Vasopressor Agents?

  • Augments contractility, after preload established, thus improving cardiac output.

  • Risk tachycardia and increased myocardial oxygen consumption if used too soon

  • Rationale, increased C.I. improves global perfusion


Vasopressors inotropic agents

Dopamine

Dobutamine

Norepinephrine

Epinephrine

Amrinone

Vasopressors & Inotropic Agents


Dopamine

Dopamine

  • Low dose (0.5 - 2 g/kg/min) = dopaminergic

  • Moderate dose (3-10 g/kg/min) = -effects

  • High dose (> 10 g/kg/min) = -effects

  • SIDE EFFECTS

    • tachycardia

    • > 20 g/kg/min  to norepinephrine


Dobutamine

Dobutamine

  • -agonist

  • 5 - 20 g/kg/min

  • potent inotrope, variable chronotrope

  • caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension


Norepinephrine

Norepinephrine

  • Potent -adrenergic vasopressor

  • Some -adrenergic, inotropic, chronotropic

  • Dose 1 - 100 g/min

  • Unproven effect with low-dose dopamine to protect renal and mesenteric flow.


Epinephrine

Epinephrine

  • - and -adrenergic effects

  • potent inotrope and chronotrope

  • dose 1 - 10 g/min

  • increases myocardial oxygen consumption particularly in coronary heart disease


Amrinone

Amrinone

  • Phosphodiesterase inhibitor, positive inotropic and vasodilatory effects

  • increased cardiac stroke output without an increase in cardiac stroke work

  • most often added with dobutamine as a second agent

  • load dose = 0.75 -1.5 mg/kg  5 - 10 g/kg/min drip

  • main side-effect - thrombocytopenia


Shock

Dilators

- inotropes

+ inotropes

Pressors


Summary pressors inotropes

Summary `pressors & inotropes

dilator

Dobutamine

Milrinone/Amrinone

Labetalol

Ca+2 blocker

ACE inhibitor

hydralazine

nitroglycerine

Nipride

-dopamine

Isuprel

Digoxin

Calcium

-blocker

- inotrope

+ inotrope

epinephrine

-dopamine

norepinephrine

pressor

neosynephrine


Case studies

CaseStudies


Shock

GSW

  • 24 year old male victim of a shotgun blast to his right lower quadrant/groin at close range.

  • Hemodynamically unstable in the field and his right lower extremity was cool and pulseless upon arrival to the trauma resuscitation area.


Shotgun blast

Shotgun Blast


Post op

Post-op

  • Patient received 12 L crystalloid, 15 units of blood, 6 units of FFP, and 2 6 packs of platelets.

  • HR 130, BP 96/48, T 34.7° C

  • PAWP 8, CVP 6, CI 4.2, SVRI 2700, LVSWI 42.

    Diagnosis? Treatment?


Shock hypovolemia

SHOCK/HYPOVOLEMIA

  • FLUIDS… FLUIDS… FLUIDS…

  • BLOOD & PRODUCTS TRANSFUSION

  • CORRECT

    • ACIDOSIS

    • COAGULOPATHY

    • HYPOTHERMIA


Shock

MVC

  • 38 year old female restrained driver who was involved in a high speed MVC.

  • She sustained a pulmonary contusion and fractured pelvis.


Icu course

ICU Course

  • Intubated and monitored with PA-C

  • PCWP = 22, CI = 3.5, SVRI = 2400, LVSWI = 39.8

  • HR = 120, BP = 110/56, SpO2 = 91, UOP = 25 cc/hr

    What do you think...


Hypovolemia

HYPOVOLEMIA

ADJUST YOUR WEDGE FOR THE PEEP


Wedge adjustment

Wedge Adjustment

  • Measured PAOP - ½ PEEP = “real PAOP”

  • PEEP = 28, therefore “real wedge” = 8


Auto pedestrian crash

Auto-Pedestrian Crash

  • Thrown from the rear bed of pick up truck during a MVC at 60 mph.

  • Hemodynamically unstable

  • Pain to palpation of the pelvis

  • Hematuria with Foley® insertion


Icu course1

ICU Course

  • Pelvis “closed”

  • QID Dressings, intubated, PA-C inserted

  • PCWP = 20, CI = 5.2, SVRI = 280, LVSWI = 24.5, PEEP = 8

    Diagnosis? Treatment?


Sepsis

Sepsis

  • Fluids

  • Correct the cause

  • Antibiotics

  • Debridement

  • Vasopressors

    • Phenylephrine

    • Levophed


Initial resuscitation

Initial Resuscitation

  • CVP: 8- 12 mm Hg

  • MAP  65 mm Hg

  • UOP  0.5 cc/kg/hr

  • Mixed venous Oxygen Sat  70%

  • Consider:

    • Transfusion to Hgb  10

    • Dobutamine up to 20 g/kg/min


Vasopressors

Vasopressors

  • Assure adequate fluid volume

  • Administer via CVL

  • Do not use dopamine for renal protection

  • Requires arterial line placement

  • Vasopressin:

    • Refractory shock

    • Infusion rate 0.01 – 0.04 Units/min


Steroid use in sepsis

Steroid Use in Sepsis

  • Refractory shock 200-300 mg/day of hydrocortisone in divided doses for 7 days

  • ACTH test

  • Once septic shock resolves, taper dose

  • Add fludrocortisone 50 g po q day


Geriatric trauma

Geriatric Trauma

  • 70 year old female

  • MVC while talking on her cell phone

  • ruptured diaphragm and spleen s/p OR

  • Intubated and PA-C


Icu course2

ICU Course

  • PCWP = 28, CI = 1.8, SVRI = 3150, LVSWI = 20.7

    Diagnosis? Treatment?


Cardiogenic shock1

Cardiogenic Shock

  • Preload augmentation - Consider Fluids

  • Contractility

    • dopamine

    • dobutamine

    • phosphodiesterase inhibitor

  • Afterload reduction

    • nitroglycerin

    • dobutamine


Don t forget

Don’t forget...

Shock: “rude unhinging of the machinery of life.”

-Samuel D. Gross, 1872


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